The microenvironment of solid tumors (TME) has critical contributions on all stages of tumorigenesis including response to treatment. Cancer associated fibroblasts (CAFs) are the most abundant cells in the TME, and through the secretion of multiple factors, they are known to be key effectors for many of the functions attributed to the TME. IKKbeta driven NF- B activation is a central driver for many inflammation-driven tumors. A pro-inflammatory NF- B gene signature in CAFs has been suggested to promote tumorigenesis in models of pancreatic, mammary skin cancer. Using an autochthonous model of colitis-associated carcinogenesis (CAC) we provide evidence for a tumor suppressive function of IKKbeta /NF- B in CAFs.